血管生成拟态研究进展

血管生成拟态(VM)是近年来发现的一种与经典的肿瘤血管生成途径完全不同、不依赖机体内皮细胞的全新肿瘤微循环模式.它描述了在高度侵袭性肿瘤组织中通过肿瘤细胞的自身变形和基质重塑形成类似血管样的通道,通过这种结构有利于肿瘤组织获取营养、侵袭和转移.血管生成拟态的提出为肿瘤研究和治疗提供了新思路.     

微血管密度与肺癌预后

目的　为研究肺癌组织内微血管密度与肺癌的生物学行为(淋巴结转移、肿瘤复发、生存时间等)的相关性。方法　我们应用SP免疫组化法研究FⅧ因子在60例肺癌组织中的表达。结果　60例肺癌患者微血管密度N     

肝细胞癌血管生成的螺旋CT动脉期同层动态扫描与α-平滑肌素免疫组织化学表达的相关性

目的针对肝细胞癌(HCC)血管生成情况,探讨螺旋CT动脉期同层动态扫描特征与α平滑肌素(ASMA)免疫组织化学(简称免疫组化)检查结果之间的相关性。方法术前33例HCC行螺旋CT动脉期同层动态扫描,绘制时间密度曲线(TDC)并计算相应参数;分析HCC强化征象。术后对标本切片进行常规苏木素伊红染色(HE)和ASMA免疫组化染色。对免疫组化染色结果和影像学发现进行相关性分析。结果将33例HCCTDC按强化峰值(PV)>80、40HU相似文献   

MSCT灌注成像对肺内肿块的定性及定量研究

目的:探讨多层CT灌注成像对肺部肿块的诊断价值并与肿瘤血管生成进行相关性分析。方法:对53例确诊的肺部结节或肿块性病变进行CT灌注成像。分析并记录血流量(BF)、血容量(BV)、平均通过时间(MTT)和毛细血管表面通透性(PS)。27例手术切除标本进行免疫组化染色,测定MVD和VEGF表达值,并与CT灌注参数进行相关性分析。结果:3组结节间BF、BV、PS值均表现为恶性>炎性>良性;恶性结节的BF、BV和PS值均显著高于良性结节,差异有极显著性意义(P<0.01);恶性与炎性结节间、炎性与良性结节间PS值差异有显著性意义(P<0.05),BF和BV值差异无显著性意义(P>0.05)。3组结节间MTT值差异无显著性意义(P>0.05)。MVD及VEGF与BF、BV及PS值之间均具有正相关性,与MTT值无明显相关性。结论:CT灌注成像能较全面地反映肺部病变的血流信息,可为肺部病变的鉴别诊断及评价肺癌血管生成提供依据。     

VEGF、bFGF在不同组织学类型膀胱癌中的表达及其与MVD的关系

目的　探讨血管内皮细胞生长因子 (VEGF)、碱性成纤维母细胞生长因子 (b FGF)在膀胱癌组织中的表达及其与组织学类型和微血管密度 (MVD)的关系。方法　用免疫组织化学方法检测 4 2例膀胱癌组织中 VEGF、b FGF的表达 , 因子相关抗原定量 MVD,原位杂交显示 VEGFm RAN。结果　膀胱癌的肿瘤细胞内可检测到 VEGFm RNA,其表达与组织学类型有关。VEGF、b FGF蛋白表达与组织学类型无关。MVD与膀胱癌组织学类型、b FGF、VEGFm RNA表达均有关。结论　 VEGF、b FGF在膀胱癌的血管形成以及发生、发展过程中起有重要作用 ,特别是 VEGFm RNA在不同组织学类型膀胱癌的表达结果 ,可较准确地表明 VEGF诱导膀胱肿瘤血管形成的能力。     

子宫内膜异位症的分子病因学研究现状

子宫内膜异位症(EMS)是子宫内膜腺体和基质种植于子宫以外的一种雌激素依赖性疾病,是引起该病患者盆腔疼痛和不孕的常见因素。EMS的发病机制迄今尚未完全阐明,是妇产科临床和基础研究的热点。目前研究认为,EMS发病的分子机制不纯粹是某一生物学特征异常,尚涉及腹膜侵袭、血管形成、细胞凋亡、细胞黏附及自噬等方面,并且某一信号通路异常,参与EMS发病过程的各个环节,而涉及整个通路调控网络异常。笔者拟从腹膜的侵袭、血管形成、细胞凋亡、细胞黏附、自噬等方面,对EMS的分子病因学最新研究进展进行阐述。     

经直肠彩色多普勒超声检测直肠癌局部血流特征与肿瘤血管生长因子表达的相关性研究

目的 探讨经直肠彩色多普勒超声检测直肠癌局部血流及其与肿瘤血管生成间的关系。方法 回顾分析了经病理证实的直肠癌患者121例，观察直肠癌病灶局部的彩色多普勒血流显像（CDFI）、能量多普勒（PDI）血流信号的变化、分布及特征，采用免疫组织化学技术检测病灶局部血管内皮生长因子（VEGF）的表达，并对血流信号和VEGF表达的阳性细胞半定量分级。结果 CDFI和PDI检查病灶局部血流信号增多，血流信号的增多似与病灶分期无关。uT1和uT2期病灶VEGF表达与CDFI和PDI呈弱相关，uT1和uT2期病灶VEGF的表达与CDFI和PDI显著相关。结论 彩色多普勒超声对病灶血流信号的分析在一定程度上可反映肿瘤病灶的血管生成特征。     

巨噬细胞移动抑制因子促进新生微血管生成

目的观察巨噬细胞移动抑制因子对体外培养的人血管内皮细胞增殖的作用,以及通过体内外血管生成实验证实巨噬细胞移动抑制因子促进新生微血管生成的作用。方法采用体外培养的人血管内皮细胞株EA-hy926为实验对象,通过四甲基偶氮唑盐比色法测定血管内皮细胞增殖;利用体外血管生成分析试剂盒量化分析巨噬细胞移动抑制因子在体外对新生微血管生成的作用;利用免疫组织化学染色法检测巨噬细胞移动抑制因子作用后基底膜类似物栓子中第Ⅷ因子相关抗原观察巨噬细胞移动抑制因子在小鼠体内对新生微血管生成的作用。结果巨噬细胞移动抑制因子可以促进体外培养的人血管内皮细胞增殖,促进体外培养的人血管内皮细胞在体外形成血管腔,在小鼠体内也能促进基底膜类似物栓子中新生微血管生成。结论巨噬细胞移动抑制因子有促进新生微血管生成的作用。     

Immunohistochemical analysis of vascular endothelial growth factor (VEGF) and p53 expression in pterygium from Tunisian patients

A pterygium is characterized by abnormal fibrovascular corneoconjunctival tissue. A number of investigations have attempted to elucidate this incompletely understood pathology. Since vascular endothelial growth factor (VEGF) and p53 are known to participate in tumor vascularization, our purpose was to study VEGF and p53 expression in active primary and recurrent pterygium from Tunisian patients. To this end, 15 cases of active primary pterygium and five cases of recurrent pterygium from Tunisia were studied by immunohistochemistry. Antibodies raised against VEGF and p53 were used to analyze the distribution and expression of these markers in pterygium and normal human conjunctiva were used as negative control. VEGF and p53 proteins were found in all cases of primary pterygium in epithelial, fibroblast and vascular endothelial cells. Active primary and recurrent pterygium have different patterns of expression. In primary pterygium, an important variability of p53 and VEGF expression was observed. However, in recurrent pterygium, p53 immunoreactivity was weak to moderate, whereas VEGF immunoreactivity was strong. In normal human conjunctiva, VEGF and p53 expression was weak to negative. The overexpression of VEGF in active primary and recurrent pterygium suggests that angiogenesis may play a role in pterygium pathogenesis and the expression of p53 in active primary pterygium, which might be associated with its mutated form, supports the hypothesis that actinic radiation may be involved in the genesis of pterygium. Thus, VEGF and p53 may be useful biomarkers for understanding the physiopathology of pterygium.     

Transplantation of SNAP-treated adipose tissue-derived stem cells improves cardiac function and induces neovascularization after myocardium infarct in rats

Stem cell therapy has been considered a promise for damaged myocardial tissue. We have previously shown that S-nitroso-N-acetyl-D,L-penicillamine (SNAP) increases the expression of several muscular markers and VEGF in mesenchymal stem cells, indicating that transplantation of SNAP-treated cells could provide better functional outcomes. Here, we transplanted SNAP-treated adipose tissue-derived stem cells (ADSCs) in rat infarcted myocardium. After 30 days, we observed a significant improvement of the ejection fraction in rats that received SNAP-treated ADSCs, compared with those that received untreated cells (p = 0.008). Immunohistochemical reactions showed an increased expression of troponin T–C and von Willebrand factor, and organized vascular units in the infarcted area of tissue transplanted with treated ADSCs. SNAP exposure induced intracellular S-nitrosation, a decreased GSH/GSSG ratio, but did not increase cGMP levels. Collectively, these results indicate that SNAP alters the redox environment of ADSCs, possibly associated with a pre-differentiation state, which may improve cardiac function after transplantation.